Search

Failure to get COVID-19 vaccines to nations with high rates of uncontrolled advanced HIV puts people living with that virus at even greater risk, and could drive the emergence of coronavirus variants. Failure to get COVID-19 vaccines to nations with high rates of uncontrolled advanced HIV puts people living with that virus at even greater risk, and could drive the emergence of coronavirus variants.

Continued uncontrolled transmission of SARS-CoV-2 in many parts of the world is creating conditions for substantial evolutionary changes to the virus1,2. Here we describe a newly arisen lineage of SARS-CoV-2 (designated 501Y.V2; also known as B.1.351 or 20H) that is defined by eight mutations in the spike protein, including three substitutions (K417N, E484K and N501Y) at residues in its receptor-binding domain that may have functional importance3,4,5. This lineage was identified in South Africa after the first wave of the epidemic in a severely affected metropolitan area (Nelson Mandela Bay) that is located on the coast of the Eastern Cape province. This lineage spread rapidly, and became dominant in Eastern Cape, Western Cape and KwaZulu–Natal provinces within weeks. Although the full import of the mutations is yet to be determined, the genomic data—which show rapid expansion and displacement of other lineages in several regions—suggest that this lineage is associated with a selection advantage that most plausibly results from increased transmissibility or immune escape6,7,8.

Background Hepatitis B virus (HBV), Human Immunodeficiency virus (HIV) and Tuberculosis (TB) are common infections in South Africa. We utilized the opportunity of care provision for HIV-TB co-infected patients to better understand the relationship between these coinfections, determine the magnitude of the problem, and identify risk factors for HBV infection in HIV infected patients with and without TB in KwaZulu-Natal, South Africa. Methods This retrospective cohort analysis was undertaken in 2018. In-care HIV infected patients were included in the analysis. Results from clinical records were analysed to determine the prevalence, incidence, persistence and factors associated with HBsAg positivity in HIV-infected patients with or without TB co-infection. Results A total of 4292 HIV-infected patients with a mean age of 34.7 years (SD: 8.8) were included. Based on HBsAg positivity, the prevalence of HBV was 8.5% (363/4292) [95% confidence interval (CI): 7.7–9.3] at baseline and 9.4% (95%CI: 8.6–10.3%) at end of follow-up. The HBV incidence rate was 2.1/100 person-years (p-y). Risk of incident HBV infection was two-fold higher among male patients (HR 2.11; 95% CI: 1.14–3.92), while severe immunosuppression was associated with a greater than two-fold higher risk of persistent infection (adjusted risk ratio (RR) 2.54; 95% CI 1.06–6.14; p = 0.004. Additionally, active TB at enrolment was associated with a two-fold higher risk of incident HBV infection (aHR 2.38; 95% CI: 0.77–7.35). Conclusion The provision of HIV care and treatment in high HBV burden settings provide a missed opportunity for HBV screening, immunization and care provision.

Cytomegalovirus pneumonia has repeatedly been described in the context of HIV-exposed uninfected and HIV-infected infants. Despite its significant role in the etiology of childhood pneumonia, there is still a paucity of literature generally, and specifically in Africa, suggesting that it might be a neglected disease. Emerging evidence highlights the importance of postnatal transmission through breastmilk. The pathogenetic significance of the multiplicity of strains acquired through repeated re-infections in early infancy is unknown. The development of cheap, accurate diagnostic tools and safe, effective antivirals and the maintenance of effective prevention and treatment of pediatric HIV are needed to manage cytomegalovirus pneumonia in low-resource settings.

Humanity is currently facing the challenge of two devastating pandemics caused by two very different RNA viruses: HIV-1, which has been with us for decades, and SARS-CoV-2, which has swept the world in the course of a single year. The same evolutionary strategies that drive HIV-1 evolution are at play in SARS-CoV-2. Single nucleotide mutations, multi-base insertions and deletions, recombination, and variation in surface glycans all generate the variability that, guided by natural selection, enables both HIV-1’s extraordinary diversity and SARS-CoV-2’s slower pace of mutation accumulation. Even though SARS-CoV-2 diversity is more limited, recently emergent SARS-CoV-2 variants carry Spike mutations that have important phenotypic consequences in terms of both antibody resistance and enhanced infectivity. We review and compare how these mutational patterns manifest in these two distinct viruses to provide the variability that fuels their evolution by natural selection. Fil: Fischer, Will. Los Alamos National Laboratory; Estados Unidos. New Mexico Consortium; México Fil: Giorgi, Elena E.. New Mexico Consortium; México. Los Alamos National Laboratory; Estados Unidos Fil: Chakraborty, Srirupa. Center For Nonlinear Studies; Estados Unidos. Los Alamos National Laboratory; Estados Unidos Fil: Nguyen, Kien. Los Alamos National Laboratory; Estados Unidos Fil: Bhattacharya, Tanmoy. Los Alamos National Laboratory; Estados Unidos Fil: Theiler, James. Los Alamos National Laboratory; Estados Unidos Fil: Goloboff, Pablo Augusto. American Museum of Natural History; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - Tucumán. Unidad Ejecutora Lillo; Argentina Fil: Yoon, Hyejin. Los Alamos National Laboratory; Estados Unidos Fil: Abfalterer, Werner. Los Alamos National Laboratory; Estados Unidos Fil: Foley, Brian T.. Los Alamos National Laboratory; Estados Unidos Fil: Tegally, Houriiyah. University Of Kwazulu-natal; Sudáfrica Fil: San, James Emmanuel. University Of Kwazulu-natal; Sudáfrica Fil: de Oliveira, Tulio. University of KwaZulu-Natal; Sudáfrica Fil: Gnanakaran, Sandrasegaram. Los Alamos National Laboratory; Estados Unidos Fil: Korber, Bette. Los Alamos National Laboratory; Estados Unidos. New Mexico Consortium; México

SummaryWhile most people effectively clear SARS-CoV-2, there are several reports of prolonged infection in immunosuppressed individuals. Here we present a case of prolonged infection of greater than 6 months with shedding of high titter SARS-CoV-2 in an individual with advanced HIV and antiretroviral treatment failure. Through whole genome sequencing at multiple time-points, we demonstrate the early emergence of the E484K substitution associated with escape from neutralizing antibodies, followed by other escape mutations and the N501Y substitution found in most variants of concern. This provides support to the hypothesis of intra-host evolution as one mechanism for the emergence of SARS-CoV-2 variants with immune evasion properties.

BACKGROUND In low- and middle-income countries, increasing levels of HIV drug resistance (HIVDR) on second-line protease inhibitor (PI)-based regimens are a cause for concern, given limited drug options for third-line antiretroviral therapy (ART). OBJECTIVES We conducted a retrospective analysis of routine HIV-1 genotyping laboratory data from KwaZulu-Natal, in South Africa, to describe the frequency and patterns of HIVDR mutations and their consequent impact on standardized third-line regimens. METHODS This was a cross-sectional analysis of all HIV-1 genotypic resistance tests conducted by the National Health Laboratory Service in KwaZulu-Natal, South Africa (Jan 2015 - Dec 2016), for adults and adolescents (age ≥10 years) on second-line PI-based ART with virological failure. We assigned a third-line regimen to each record, based on a national treatment algorithm and calculated the genotypic susceptibility score (GSS) for that regimen. RESULTS Of 348 samples analyzed, 287 (83%) had at least one drug resistance mutation (DRM) and 114 (33%) had at least one major PI DRM. Major PI resistance was associated with longer duration on second-line ART (aOR per 6-months, 1.11, 95% CI 1.04-1.19) and older age (aOR 1.03, 95% CI 1.01-1.05). Of 112 patients requiring third-line ART, 12 (11%) had a GSS of

SummaryContinued uncontrolled transmission of the severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2) in many parts of the world is creating the conditions for significant virus evolution. Here, we describe a new SARS-CoV-2 lineage (501Y.V2) characterised by eight lineage-defining mutations in the spike protein, including three at important residues in the receptor-binding domain (K417N, E484K and N501Y) that may have functional significance. This lineage emerged in South Africa after the first epidemic wave in a severely affected metropolitan area, Nelson Mandela Bay, located on the coast of the Eastern Cape Province. This lineage spread rapidly, becoming within weeks the dominant lineage in the Eastern Cape and Western Cape Provinces. Whilst the full significance of the mutations is yet to be determined, the genomic data, showing the rapid displacement of other lineages, suggest that this lineage may be associated with increased transmissibility.

Occult hepatitis B virus (HBV) infection (OBI) is defined as the presence of HBV DNA in the liver with or without detectable HBV DNA in the serum of individuals testing HBV surface antigen (HBsAg) negative using currently available assays. The prevalence of OBI among patients receiving hemodialysis (HD) treatment remains poorly characterized in South Africa despite the high prevalence of HBV. We sought to determine the prevalence of OBI in HD units in tertiary hospitals of KwaZulu-Natal and to characterize the HBV S gene mutations potentially responsible for OBI. A cross-sectional descriptive study of residual diagnostic plasma samples from 85 HBsAg-negative patients receiving HD treatment was included. The PreS/S gene was amplified with a nested HBV polymerase chain reaction for downstream next-generation sequencing, to determine the viral genotype and identify S gene mutations associated with OBI. Nine of the 85 samples had OBI, based on detectable HBV DNA. The point prevalence of OBI was 10.6% (95% control interval: 5.5%-19.1%). Phylogenetic analysis of the samples with OBI showed that all belonged to genotype A. Three (~33%) samples had mutations in the major hydrophilic region (MHR) within the S gene, three (~33%) had mutations within the S gene but outside the MHR, whilst the remaining three had no mutations observed. The prevalence of OBI in HBsAg-negative patients undergoing HD was 10.6%, suggesting that OBI is a clinically significant problem in patients with HD in this region. The screening methods for HBV infection need to be revised to include nucleic acid testing.